Liver, biliary & pancreas Flashcards
Describe the potential effects on the liver of long-term excessive alcohol ingestion
- Steatosis: fatty change, perivascular fibrosis
- Hepatitis: liver cell necrosis, inflammatory response, Mallory bodies, fatty change, fibrosis
- Cirrhosis: extensive fibrosis, hyperplastic nodules
- (Hepatocellular carcinoma)
What are the possible sequelae of cirrhosis?
Portal HTN, GIT bleeding, hepatic failure, coagulopathy, hepatocellular carcinoma, hepatorenal syndrome, encephalopathy, infection
Describe the pathogenesis of acute calculous cholecystitis
- Chemical irritation of the gallbladder by retained bile acids
- Release of inflammatory mediators - lysolecithin, PGs
- GB dysmotility
- In severe cases, ischaemia from distension and increased luminal pressures compromising mucosal blood flow
- Bacterial contamination (late complication)
How does the pathogenesis of acalculous cholecystitis differ from calculous cholecystitis?
- Less common (10%) and assoc with severly il patients
- Ischaemia due to diminished flow in end arterial cystic artery circulation
- Occurs in sepsis with hypotension and MOF, immunosuppresion, major trauma or burns, DM or infections
What are the features of the different hepatitis viruses causing hepatitis A, B, C and D?
Organism:
Hep A - ssRNA, hepatovirus (picornavirus), hep B - partially dsDNA, hepadnavirus, hep C - ssRNA, flaviviridae, hep D - circular defective ssRNA, subviral particle deltaviridae
Route of transmission:
Hep A - faecal-oral, hep B - parenteral, sexual contact, perinatal, hep C - parenteral, intranasal cocaine, hep D - parenteral
Mean incubation period:
Hep A 2-4 wks, hep B 1-4 mths, hep C 7-8 wks, hep D same as HBV
Frequency of CLD:
Hep A never, hep B 10%, hep C 80%, hep D 5% (co-infection), ≤70% superinfection
What are the risk factors for acquiring hepatitis C?
IVDU 54%, multiple sexual partners 36%, recent surgery 16%, needle stick 10%, multiple contacts with HCV infected person 10%, HCW 1.5%, perinatal 6% (cf HBV 20%), unknown 32%
What are the potential outcomes of HCV infection?
- Acute infection generally asymptomatic, rarely fulminant hepatitis
- 85% progress to chronic persistent hepatitis
- 15% resolve completely
- 20% chronic infection progress to cirrhosis
- Some may develop HCC
What are the potential causes of acute pancreatitis?
- Metabolic - alcoholism, hyperlipoproteinaemia, hyperCa, drugs e.g. azathioprine
- Genetic - mutations in PRSS1 and SPINK1 genes
- Mechanical - gallstones, trauma, iatrogenic injury (surgery, ERCP)
- Vascular - shock, atheroembolism, vasculitis
- Infections - mumps
Describe the pathogenesis of acute pancreatitis
Autodigestion by inappropriately activated pancreatic enzymes
Trypsinogen activated to trypsin which in turn activates prophospholipase & proelastase, prekallikrein then kinin system, and Hageman factor then activated clotting and complement systems
Mechanisms underlying pancreatic enzyme activation:
- Pancreatic duct obstruction
- Primary acinar cell injury
- Defective intracellular transport of proenzymes
- Alcohol - direct toxic effect on pancreatic acinar cells
What are the acute complications of sever pancreatitis?
Hameolysis, DIC, fluid sequestration, ARDS, diffuse fat necrosis, peripheral vascular collapse, shock, ATN
What are the causes of portal hypertension?
Increased resistance to portal blood flow:
- Prehepatic - portal venous thrombosis or narrowing
- Hepatic* - cirrhosis, massive fatty change, schistosomiasis, granulomatous disease (e.g. sarcoid, TB)
- Posthepatic - severe RHF, constrictive pericarditis, hepatic vein occlusion
What are the clinical consequences of portal hypertension?
Ascites - with potential for infection
Portosystemic shunts - varices, haemarrhoids, spider naevi
Congestive splenomegaly - thrombocytopaenia, pancytopaenia
Hepatic encephalopathy
